Page 115 - Clinical Small Animal Internal Medicine

11 Hypoadrenocorticism in Dogs and Cats 83

patient with clinical signs consistent with hypoadreno- patients, but often occur in anuric and oliguric AKI
VetBooks.ir corticism. Electrolyte analysis must be included in the dogs. Addisonians may initially present with physiologic
oliguria (appropriately decreased urine production in
minimum database, as sodium and potassium abnormal-
ities are often the first specific indicators of HOAC, and
rehydration results in polyuria. Thus, if a hypovolemic,
electrolyte disturbances are common in patients with the face of hypovolemia and/or dehydration). However,
gastrointestinal signs of any etiology, and need to be azotemic, hyperkalemic, hyponatremic dog has signifi-
addressed during treatment. cant improvement of attitude and becomes polyuric
upon rehydration, HOAC should be strongly considered
Serum Biochemistry, Urinalysis, and Complete as a differential diagnosis.
Blood Count Hypocholesterolemia and hypoalbuminemia occur in
Most dogs with HOAC are hyperkalemic and hypona- approximately 10% and 15% dogs with HOAC, respec-
tremic at diagnosis. Dogs with “atypical” hypoadreno- tively. Both might be due to decreased hepatic produc-
corticism are not (see Atypical Hypoadrenocorticism tion and GI malabsorption. GI blood loss exacerbates the
later). Potassium concentrations usually remain below hypoalbuminemia in some cases.
8 mEq/L, but may be as high as 11 mEq/L. Sodium con- Hypoglycemia is present in about 15% of HOAC
centrations are usually 120–140 mEq/L, but may be as dogs, probably due to decreased gluconeogenesis and
low as 100 mEq/L. Some dogs present with one abnor- increased insulin sensitivity. It is usually subclinical, but
mality without the other (e.g., hyponatremia without occasionally can be severe enough to result in seizures.
hyperkalemia). Hypochloremia follows hyponatremia in Thus, hypoadrenocorticism should be a differential diag-
about half the patients. Metabolic acidosis is also com- nosis in adult dogs with unexplained hypoglycemia.
mon, due to the inability to excrete H+ ions from the dis- Total and ionized hypercalcemia occurs in about 30%
tal tubule. of Addisonians. It is not usually the presenting com-
Electrolyte abnormalities are not always detected early plaint, but HOAC should be considered a differential
in the course of the disease, and may appear as disease diagnosis in hypercalcemic patients.
progresses. Emphasis is sometimes placed on calculation Increased alanine aminotransferase (ALT), alkaline
of the Na+/K+ ratio. The lower the sodium and the phosphatase (ALP), and aspartate aminotransferase
higher the potassium concentration, the lower the ratio. (AST) are also frequently seen (20–30%) in HOAC
Although lower ratios make HOAC more likely, a high dogs, possibly secondary to hepatic hypoperfusion and
ratio does not rule it out, and dogs with low ratios do not cholestasis.
always have HOAC. Therefore, the utility of the ratio is At diagnosis, about 30% of Addisonian dogs are ane-
questionable. Any dog with hyponatremia and/or hyper- mic. This increases to 70% following rehydration. It is
kalemia should be considered a suspect for HOAC, usually a mild normochromic, normocytic, nonregen-
regardless of the ratio. erative anemia, and GI blood loss should be suspected
Most patients experience some degree of azotemia, in patients with severe anemia. The lack of a stress
with increased BUN (90% of dogs) and creatinine (65%). leukogram (neutrophilia, lymphocytosis, monocytosis,
This is due to a combination of decreased renal perfu- and eosinopenia) in a sick dog is suggestive of HOAC.
sion from hypovolemia, and GI blood loss (increased Occasionally, lymphocytosis and eosinophilia occur
BUN). Phosphorus is usually increased, as well. Although (10%), but neutropenia is rare.
the azotemia is primarily pre-renal in nature, most dogs
with HOAC have a urine specific gravity <1.030 (often Diagnostic Imaging
<1.020), which is more dilute than expected with pre- Diagnostic imaging is not required to diagnose HOAC in
renal azotemia alone. For this reason, and the presence of most patients, but abdominal imaging is often performed
hyperkalemia and hyponatremia, some Addisonian in the initial work‐up of patients with gastrointestinal
patients are initially misdiagnosed with acute kidney signs. Imaging is recommended, however, in Addisonian
injury (AKI). Given the difference in prognosis and treat- patients that do not respond to appropriate therapy. These
ment, clinicians must consider HOAC in every suspected patients may have concurrent disease or HOAC due to
AKI patient, especially if the dog has a history of gastro- infiltrative disease (e.g., neoplasia or fungal disease invad-
intestinal signs. Severe azotemia caused by HOAC usu- ing the adrenal cortex).
ally resolves quickly following appropriate rehydration. In patients with primary idiopathic HOAC, abdominal
Primary renal damage is possible with prolonged hypo- radiographs and ultrasound may reveal a small liver, con-
volemia, but most Addisonian patients recover renal sistent with hypovolemia. Adrenal gland length and thick-
function. Conversely, patients with AKI take much ness might be smaller than in normal dogs, but the overlap
longer or never improve. Additionally, significant hyper- in adrenal size between normal and HOAC patients does
kalemia and hyponatremia rarely occur in polyuric AKI not allow definitive differentiation. Thoracic radiographs